Endothelial Dysfunction Is Associated with Cerebrovascular Events in Pre-Dialysis CKD Patients: A Prospective Study.
cardiovascular risk
cerebrovascular events
chronic kidney disease
endothelial dysfunction
peripheral arterial tonometry
reactive hyperemia index
Journal
Life (Basel, Switzerland)
ISSN: 2075-1729
Titre abrégé: Life (Basel)
Pays: Switzerland
ID NLM: 101580444
Informations de publication
Date de publication:
07 Feb 2021
07 Feb 2021
Historique:
received:
28
12
2020
revised:
01
02
2021
accepted:
01
02
2021
entrez:
10
2
2021
pubmed:
11
2
2021
medline:
11
2
2021
Statut:
epublish
Résumé
Patients with chronic kidney disease (CKD) have markedly increased rates of end stage renal disease, major adverse cardiovascular/cerebrovascular events (MACCEs), and mortality. Endothelial dysfunction (ED) is an early marker of atherosclerosis that is emerging as an increasingly important non-traditional cardiovascular risk factor in CKD. There is a lack of clinical studies examining the association between ED and both cardiovascular and renal endpoints in patients with CKD. We examined the association between reactive hyperemia index (RHI), a validated measure of endothelial function measured by peripheral arterial tonometry (PAT), with traditional cardiovascular risk factors in pre-dialysis CKD patients and prospectively evaluated the role of RHI as predictor of renal and cardiovascular outcomes in this population. One hundred and twenty pre-dialysis patients with CKD stages 1 to 5 (CKD group) and 18 healthy kidney donor candidates (control group) were recruited and had a successful RHI measurement by PAT. General demographic and clinical information including traditional cardiovascular risk factors were registered from all participants. Thereafter, patients were prospectively followed-up for a median time of 47 (IQR 19-66) months to determine associations of RHI with renal outcomes, MACCEs, hospitalizations or mortality. In the CKD patient population, the mean age was 57.7 ± 15.5 years, the mean eGFR was 54.9 ± 36.7 mL/min/1.73 m
Sections du résumé
BACKGROUND
BACKGROUND
Patients with chronic kidney disease (CKD) have markedly increased rates of end stage renal disease, major adverse cardiovascular/cerebrovascular events (MACCEs), and mortality. Endothelial dysfunction (ED) is an early marker of atherosclerosis that is emerging as an increasingly important non-traditional cardiovascular risk factor in CKD. There is a lack of clinical studies examining the association between ED and both cardiovascular and renal endpoints in patients with CKD.
AIMS
OBJECTIVE
We examined the association between reactive hyperemia index (RHI), a validated measure of endothelial function measured by peripheral arterial tonometry (PAT), with traditional cardiovascular risk factors in pre-dialysis CKD patients and prospectively evaluated the role of RHI as predictor of renal and cardiovascular outcomes in this population.
METHODS
METHODS
One hundred and twenty pre-dialysis patients with CKD stages 1 to 5 (CKD group) and 18 healthy kidney donor candidates (control group) were recruited and had a successful RHI measurement by PAT. General demographic and clinical information including traditional cardiovascular risk factors were registered from all participants. Thereafter, patients were prospectively followed-up for a median time of 47 (IQR 19-66) months to determine associations of RHI with renal outcomes, MACCEs, hospitalizations or mortality.
RESULTS
RESULTS
In the CKD patient population, the mean age was 57.7 ± 15.5 years, the mean eGFR was 54.9 ± 36.7 mL/min/1.73 m
Identifiants
pubmed: 33562195
pii: life11020128
doi: 10.3390/life11020128
pmc: PMC7915587
pii:
doi:
Types de publication
Journal Article
Langues
eng
Références
J Am Coll Cardiol. 2002 Jan 16;39(2):257-65
pubmed: 11788217
Lancet Neurol. 2014 Aug;13(8):823-33
pubmed: 25030514
J Appl Physiol (1985). 2006 Aug;101(2):545-8
pubmed: 16614356
N Engl J Med. 2004 Sep 23;351(13):1296-305
pubmed: 15385656
Nephron. 2016;134(3):167-171
pubmed: 27576317
J Am Coll Cardiol. 1995 Nov 1;26(5):1235-41
pubmed: 7594037
Toxins (Basel). 2020 Jun 18;12(6):
pubmed: 32570781
J Am Coll Cardiol. 2004 Dec 7;44(11):2137-41
pubmed: 15582310
J Am Heart Assoc. 2014 Dec 15;3(6):e001279
pubmed: 25510401
Lancet. 2012 Nov 10;380(9854):1649-61
pubmed: 23013600
Clin Exp Nephrol. 2010 Dec;14(6):558-70
pubmed: 20700621
Hypertens Res. 2015 Mar;38(3):193-8
pubmed: 25471235
Am J Cardiol. 2014 Jan 1;113(1):162-7
pubmed: 24169007
PLoS One. 2015 Jul 01;10(7):e0132047
pubmed: 26132137
BMC Nephrol. 2019 Jul 30;20(1):288
pubmed: 31362711
Kidney Int. 2002 Apr;61(4):1486-94
pubmed: 11918756
Circulation. 1995 Mar 1;91(5):1314-9
pubmed: 7867167
J Am Coll Cardiol. 2012 Oct 30;60(18):1778-86
pubmed: 23040568
J Vis Exp. 2010 Oct 15;(44):
pubmed: 20972417
Arch Intern Med. 2004 Mar 22;164(6):659-63
pubmed: 15037495
Int J Cardiol. 2014 May 15;173(3):481-6
pubmed: 24703800
Ren Fail. 2011;33(4):411-7
pubmed: 21529270
Cerebrovasc Dis. 2011;32(2):155-62
pubmed: 21778713
Eur Heart J. 2010 May;31(9):1142-8
pubmed: 20181680
Circulation. 2008 May 13;117(19):2467-74
pubmed: 18458169
J Clin Med. 2020 Jul 23;9(8):
pubmed: 32718053
Int J Cardiol. 2013 Sep 20;168(1):344-51
pubmed: 23041097
JAMA. 2014 Dec 3;312(21):2234-43
pubmed: 25402757
Nephron Extra. 2012 Jan;2(1):283-92
pubmed: 23243413
Nephrol Dial Transplant. 2008 Mar;23(3):959-65
pubmed: 17984105
Int J Vasc Med. 2012;2012:904141
pubmed: 22500237
J Am Soc Nephrol. 2004 May;15(5):1307-15
pubmed: 15100371
Circ Res. 2016 Feb 19;118(4):620-36
pubmed: 26892962
Lancet. 2012 Nov 10;380(9854):1662-73
pubmed: 23013602
J Am Heart Assoc. 2013 Nov 25;2(6):e000426
pubmed: 24275629
J Cardiovasc Pharmacol. 2001 Nov;38 Suppl 2:S75-8
pubmed: 11811384